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• W1633947760 abstract "In vivo, gastric infection with Helicobacter pylori leads to substantial production of the inflammatory cytokines IL-1, IL-6, TNF-alpha, and IL-8. H. pylori strains that contain the cag pathogenicity island (cag+) and are associated with ulceration and gastric carcinoma induce greater cytokine production than cag- strains. Expression of these cytokines is often regulated by the transcription factor complex, nuclear factor-kappa B (NF-kappa B) through kappa B-binding elements in the enhancer/promoter regions of their genes. We report that more virulent cag+ H. pylori strains induce increased NF-kappa B-DNA binding activity, which elevates IL-8 expression in AGS gastric epithelial cells. The cag+ H. pylori strains induce significant stimulation of IL-8 promoter-driven reporter activity, while cag- strains do not. Furthermore, mutation of specific genes within the cag island (picA1 and picB) ablates enhanced NF-kappa B activation and IL-8 transcription. Increased IL-8 expression is inhibited by mutation in either the NF-kappa B or NF-IL-6 binding element. The cag+ strains, compared with the cag- strains, induce enhanced nuclear localization of a RelA-containing NF-kappa B binding complex, but no increase in NF-IL-6 binding activity. These studies demonstrate that the ability of different types of H. pylori strains to activate NF-kappa B correlates with their ability to induce IL-8 transcription and indicate a mechanism for the heightened inflammatory response seen in subjects infected with cag+ H. pylori strains." @default.
• W1633947760 created "2016-06-24" @default.
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• W1633947760 date "1998-03-01" @default.
• W1633947760 modified "2023-10-06" @default.
• W1633947760 title "Activation of IL-8 gene expression by Helicobacter pylori is regulated by transcription factor nuclear factor-kappa B in gastric epithelial cells." @default.
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• W1633947760 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/9498783" @default.
• W1633947760 hasPublicationYear "1998" @default.
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